PubMed · 11613434
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V Roelcke. 1996. [Not Available].. https://pubmed.ncbi.nlm.nih.gov/11613434/
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Infectious diseases are the confrontation of two worlds, the microbial world and the world of human physiology. Although these two worlds are as a whole governed by the same laws of nature, they show substantial differences: the microbiological world is 1000 times older, and was initiated by the development of the archaea, the 'living organisms of the extreme': its biomass and its diversity are immense - two to three billion species or 60% of the total biomass of the planet. The number of pathogens that adapted to man, however, is extremely limited - barely 1000. Thus, over billions of years, an evolution of the microbial world took place from 'early life', characterized by chemosynthesis, to the 'modern pathogens', and entailed a dramatic 'concentration' of life conditions and an adaptation towards a narrow range of requirements - those allowing survival in the human body. Within the last two centuries, these two slowly evolving systems, microbial life and human life, were profoundly modified in an unprecedented manner by a third player, human civilization, with its global impact on the environment through physical, chemical, societal, and climatic determinants. An appreciation of the evolution of infectious diseases in the 21st century and of the development of new diagnostic and therapeutic strategies therefore requires a full understanding of these three domains: human physiology, microbiology, and the environment. This review will put major emphasis on the environmental role of civilization on infectious diseases before considering new opportunities to combat them through novel and creative solutions.
Compensatory hyperinsulinemia stemming from peripheral insulin resistance is a well-recognized metabolic disturbance that is at the root cause of diseases and maladies of Syndrome X (hypertension, type 2 diabetes, dyslipidemia, coronary artery disease, obesity, abnormal glucose tolerance). Abnormalities of fibrinolysis and hyperuricemia also appear to be members of the cluster of illnesses comprising Syndrome X. Insulin is a well-established growth-promoting hormone, and recent evidence indicates that hyperinsulinemia causes a shift in a number of endocrine pathways that may favor unregulated tissue growth leading to additional illnesses. Specifically, hyperinsulinemia elevates serum concentrations of free insulin-like growth factor-1 (IGF-1) and androgens, while simultaneously reducing insulin-like growth factor-binding protein 3 (IGFBP-3) and sex hormone-binding globulin (SHBG). Since IGFBP-3 is a ligand for the nuclear retinoid X receptor alpha, insulin-mediated reductions in IGFBP-3 may also influence transcription of anti-proliferative genes normally activated by the body's endogenous retinoids. These endocrine shifts alter cellular proliferation and growth in a variety of tissues, the clinical course of which may promote acne, early menarche, certain epithelial cell carcinomas, increased stature, myopia, cutaneous papillomas (skin tags), acanthosis nigricans, polycystic ovary syndrome (PCOS) and male vertex balding. Consequently, these illnesses and conditions may, in part, have hyperinsulinemia at their root cause and therefore should be classified among the diseases of Syndrome X.
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